Breathing

In late pregnancy the tidal volume increases by 20% at 12 weeks and by 30–50% at 40 weeks. Because the total lung capacity is unchanged, this increase in tidal volume is at the expense of a proportionate decrease in inspiratory and expiratory reserve, and residual capacity is decreased by up to 25%. Therefore, the patient will have a reduced ability to compensate for any increase in oxygen demand due to illness or injury.

Indeed, the normal physiological demands of pregnancy result in an increase in oxygen demand of 20% in the well obstetric patient. This is met by a small increase in respiratory rate of approximately 1–2 breaths per minute as well as the increased tidal volume.

The shape of the rib cage changes, splaying out at its base due to the need to accommodate a gravid uterus. This reduces costal excursion and so the diaphragm plays an increasingly significant role in supporting respiration as the pregnancy progresses.

During labour and delivery there is an increase in hyperventilation due to pain and anxiety, and in particular during the effort exerted during the second stage of labour.

Circulation

Blood volume rises throughout pregnancy, and by the last trimester it will have increased by up to 50%. This increase can be even greater in women with a multiple pregnancy. Red blood cell numbers also rise, but since this is to a lesser degree than plasma volumes, the actual haemoglobin concentration falls. This results in a dilutional anaemia (or haemodilution) compared with the non‐pregnant state, and a subsequent reduced capacity for carrying oxygen.

By the middle of pregnancy, cardiac output rises by approximately 40% due largely to an increase in the stroke volume. This is also due, to a lesser extent, to an increase in the pulse rate to about 85–100 bpm at the end of the third trimester. However, the workload of the heart is not increased due to the reduction in blood viscosity (as a result of haemodilution) and decreased peripheral vascular resistance (reduced afterload).

Cardiac output increases due to:

• Hormone‐mediated peripheral vasodilatation
  
• Greater metabolic requirements arising from increased organ size and activity (particularly relating to the lungs, kidneys, gastrointestinal system and skin)
  
• Increased heat production (resulting in vasodilatation in the skin)
  
• The placenta’s function as a shunt between the arterial and venous systems (the lack of a capillary system where branches of the uterine artery connect directly to the placental venous sinuses results in a lowered peripheral resistance)

The reduction in peripheral vascular resistance places obstetric patients at risk of postural hypotension due to the potential for a sudden drop in systolic blood pressure when moving to a standing position. This may result in cerebral hypoperfusion and, consequently, syncope. To avoid this risk, obstetric patients should be encouraged to move from a lying to sitting or sitting to standing position slowly. For example, if they are moving from lying to standing they should:

• Sit up with their legs out straight
  
• Wait for a few seconds and then check for dizziness
  
• Move so that their legs are bent over the edge of the bed
  
• Wait for a few seconds and then check for dizziness
  
• Stand up

At the beginning of pregnancy, the systolic blood pressure falls, but returns to near normal levels at term. Despite this, the pulse pressure increases due to a relatively greater fall in diastolic pressure. As in all patients, the systolic blood pressure provides a more useful indicator of patient status than the diastolic, with the exception that diastolic pressure is as important as systolic pressure in hypertension. The diastolic pressure should be documented at the point the sounds disappear (Korotkoff phase V). Occasionally in pregnancy, the sounds may not disappear. In that circumstance, diastolic blood pressure can be estimated by noting when the sounds become muffled (Korotkoff phase IV) (see Chapter 6).

Varicose veins often occur in the legs due to an increase in venous pressure, relaxation of the smooth muscle of the veins due to the effects of progesterone, and the presence of peripheral oedema. Changes in blood viscosity, venous stasis and impaired venous return during pregnancy increase the risk of venous thromboembolism.

During the late second and third trimester of pregnancy, if the patient lays flat on her back, the gravid uterus can result in supine hypotension due to aortocaval compression. The weight of the uterus compresses the inferior vena cava reducing venous return, in turn reducing cardiac filling and causing a fall in cardiac output. In response, arterial vasoconstriction occurs but arterial pressure will nevertheless fall if vena caval compression is not rapidly corrected, and the resulting low intra‐aortic pressure will allow the aorta to be compressed. The effect on the patient is maternal syncope due to reduced cerebral perfusion, and fetal hypoxia due to uterine hypoperfusion. In pre‐existing low‐output states such as hypovolaemic shock or chest compressions during cardiac arrest, the net result may be little or no maternal and fetal circulation.

After 20 weeks of pregnancy women should NEVER be laid flat on their back. Encourage a position of comfort (semi‐recumbent) or full left lateral position for conscious patients ( Figure 5.1 ).